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Endo/Repro > 03b: Thyroid > Flashcards

03b: Thyroid Flashcards

1
Q

Major secretory product of thyroid gland is (X).

A

X = T4 (thyroxine)

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2
Q

(T4/T3/rT3) are active forms. Which of these are produced exclusively in thyroid gland?

A

T3;

T4 (T3 and rT3 can be produced from T4 in peripheral tissues)

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3
Q

(X) enzymes in peripheral tissues catalyze production of (T3/rT3/T4) from (T3/rT3/T4).

A

X = 5’-deiodinases;
T3 or rT3;
T4

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4
Q

T/F: Most circulating T3 is formed from degradation of T4, not from biosynthesis.

A

True

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5
Q

T4 biosynthesis: two coupled (X) rings form (Y).

A 
X = Tyr
Y = thyronine
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6
Q

TRH is formed in (X) and carried to (Y) cells to induce TSH secretion. Is TRH a clinically useful measurement of thyroid function?

A 
X = PVN of hypothalamus
Y = thyrotropes (of ant pit)

No - conc too low in peripheral circulation

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7
Q

Most important regulator of TRH production:

A

Long-loop negative feedback by T3/T4

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8
Q

List the four hormones, released from (X), that have same alpha and different beta subunits.

A

X = anterior pituitary;

LH, FSH, TSH, hCG

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9
Q

Most negative feedback control regulating Thyroid hormone levels takes place between (thyroid/pituitary) and (pituitary/hypothalamus).

A

Thyroid and pituitary

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10
Q

Within the thyrotrope, (T3/rT3/T4) is the hormone that produces negative feedback effects. Most of it comes from (X).

A

T3;

X = intra-pituitary conversion of T4 to T3

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11
Q

(T3/T4) negative feedback within thyrotrope has which mechanism?

A

T3;

Binds nuclear receptors and inhibits expression of both TSH subunits

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12
Q

List the levels at which glucocorticoids (stimulate/inhibit) thyroid axis.

A

Inhibit;

  1. TRH synthesis
  2. Thyrotrope responsiveness to TRH
  3. Deiodinase activity
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13
Q

Under intense TSH stimulation, you’d expect the thyroid follicle to appear:

A

Hyperplastic (shrunken); colloid undergoing resorption for hormone synthesis

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14
Q

Thyroid hormone biosynthesis requires which two components?

A
  1. Thyroglobulin

2. Iodide

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15
Q

Iodide enters thyroid follicular cell via (X). This is a(n) (uphill/downhill) movement.

A

X = Na/I symporter (NIS)

Uphill (very high iodide conc in cell compared to out)

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16
Q

Which transport proteins/pumps are present on (apical/basal) membrane of thyroid follicular cell to allow iodide entry?

A

Basal;

  1. NIS (symporter)
  2. Na/K Pump (too keep Na low in cell)
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17
Q

T/F: Iodide entry into follicular cell is rate-limiting step of thyroid hormone production.

A

True

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18
Q

TPO (thyroid peroxidase) is key enzyme that catalyzes which steps in thyroid hormone synthesis?

A
  1. Oxidization of iodide (to iodine)
  2. Incorporation into thyroglobulin
  3. Coupling (ex: T2 and T2 to form T4)
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19
Q

Immediately (before/after) exiting (apical/basal) membrane of follicular cell, iodide is (oxidized/reduced) to (X).

A

After; apical;
Oxidized
X = iodine
(by TPO enzyme)

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20
Q

The iodide attaches to (X) residues of thyroglobulin.

A

X = Tyr

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21
Q

Thyroid hormone synthesis: The actions of TPO are mediated by (X), which is generated by (Y).

A 
X = H2O2
Y = NADPH oxidase
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22
Q

Iodide transport across apical membrane of follicular cell is via (X) channel/ATPase/transporter.

A

X = Pendrin (I/Cl antiporter)

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23
Q

Tyrosine organification/iodination yields which products?

A
  1. MIT (T1) or

2. DIT (T2)

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24
Q

Thyroid colloid stores enough organified thyroglobulin for (X) period of time.

A

X = 2-3 months

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25
Q

T/F: When thyroid hormone is needed, biosynthesis of thyroglobulin starts de novo and stored iodide (in colloid) is available.

A

False - colloid stores months’ worth of already organified thyroglobulin

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26
Q

Upon stimulation of thyroid gland, follicular cells endocytose (X), which fuse with (Y). Finally, (Z) process forms mature thyroid hormones.

A 
X = colloid
Y = intracellular lysosomes
Z = proteolysis of thyroglobulins
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27
Q

Thyroid hormone synthesis: following proteolysis in lysosome, (X) enter circulation. What’s the fate of the byproducts?

A

X = mature hormones (T3/T4)

MIT, DIT stay in follicular cell and deiodinated (by thyroid deiodinase); recycling

28
Q

Most of the iodide used in thyroid hormone synthesis comes from:

A

Recycling of MIT, DIT iodides following their deiodination

29
Q

Perchlorate, a competitive inhibitor of NIS transporter, can be administered clinically to treat:

A

Hyperthyroidism (since it slows down thyroid hormone production)

30
Q

The Wolff-Chaikoff effect is essentially (stimulation/inhibition) of (X) in response to (Y).

A

Inhibition;
X = TPO
Y = high circulating iodide

31
Q

The Wolff-Chaikoff effect typically lasts how long? What’s the mechanism that causes escape from this effect?

A

A few days;

Down-regulation of NIS allows thyroid to adjust to high iodide levels (and TPO inhibition is released)

32
Q

About (X) T4 and (Y) T3 are secreted daily.

A 
X = 80-100 micrograms
Y = 5 micrograms
33
Q

Majority of T4/T3 in plasma is (free/bound).

A

Bound to TBG, albumin, or transthyretin

34
Q

The metabolic rate of many tissues is determined by the (free/bound) fraction of T3/T4.

35
Q

T/F: Physiological thyroid status best correlates with T3/T4 that’s bound to TBG, not albumin.

A

False - free hormone fraction

36
Q

T/F: Thyroid hormones are transported into target cells via passive diffusion.

A

False - via membrane carriers

37
Q

T/F: Rate-limiting step of thyroid hormone action is transport into target cell.

38
Q

Once inside target cell, thyroid hormone binds (X) receptors, in conjunction with (Y).

A 
X = non-histone protein nuclear receptors
Y = TRE (thyroid hormone response elements)
39
Q

List some proteins with genes that are regulated by T3.

A
  1. T3’s own receptor (and TRE)
  2. TRH, TSH
  3. GH
  4. Myosin heavy chain
40
Q

Certain tissues, such as (X), with (many/few) (Y), have significant response to T3 and large changes in protein synthesis/enzyme patterns.

A

X = liver
Many;
Y = nuclear receptors for T3

41
Q

List the two key ways that myocardial tissues respond to T3.

A
  1. Increasing adrenergic receptors

2. Increasing actomyosin ATPase activity

42
Q

T/F: Only the active thyroid hormone (T3) enters the target cell.

A

False - T4 enters too (encounters intracellular deiodinases that convert it to T3)

43
Q

T/F: Only the active thyroid hormone (T3) enters the target cell nucleus.

44
Q

T/F: Intracellular deiodinases (in target cell) only work on T4 (to produce T3).

A

False - also cleave T3 to T2/rT3 or T4 to rT3

45
Q

T3 effect: (increase/decrease) bone formation/maturation.

46
Q

T3 effect: (increase/decrease) oxygen consumption, BMR, and heat production.

47
Q

T3 effect: (increase/decrease) CO and ventilation. (Up/down)-regulation of (X) adrenergic receptors.

A

Increase;
Up-regulation;
X = beta

48
Q

T3 effect: increase in which processes in skeletal muscle?

A

Glycogenolysis and protein catabolism

49
Q

T3 effect: increase cholesterol (synthesis/degradation) and (increase/decrease) LDL clearance/receptors.

A

Synthesis;

Increase

50
Q

T/F: Thyroid hormone normally stimulates exclusively catabolic pathways.

A

False - both anabolic and catabolic pathways (supports balance)

51
Q

T3 effect: there’s a(n) (increase/decrease) in need for fuel. This is met by (increase/decrease) in which factors?

A

Increase; increase

  1. GI motility/absorption
  2. Increase appetite
52
Q

T/F: Like sympathetic stimulation, TPR increases with increase in T3.

A

False - T3 increases production of vasodilatory metabolites and TPR falls

53
Q

T/F: Normal whole body growth cannot occur without adequate T3 levels, even if GH is normal.

54
Q

A hypothyroid child will have a bone age that’s (more/less) than chronological age.

55
Q

Untreated (hyper/hypo)-thyroidism in children can lead to which brain impairment?

A

Hypo;

Severe, irreversible mental retardation

56
Q

Fetal thyroid gland forms (early/late) in (X) trimester. By (Y) stage, the fetal hypo-pit-thyroid axis is fully operational.

A

Early;
X = first
Y = mid-gestation

57
Q

During development, fetus receives (T3/T4/TSH) from mother/placenta to supply its needs. Thus, maternal (X) levels increase to meet greater demands.

A

T3 and T4;

Iodide and thyroid hormone

58
Q

The (increase/decrease) in thyroid hormone output during pregnancy is not met with (hyper/hypo)-thyroidism. Why?

A

Increase; hyper

Increase in TBG (due to estrogen) to bind the increased hormone levels

59
Q

Early in pregnancy, it’s actually (X) hormone that stimulates thyroid to secrete.

A

X = hCG (not TSH)

60
Q

First trimester of pregnancy: (increase/decrease) hCG, (increase/decrease) TSH, (increase/decrease) thyroid hormones.

A

Increase;
Decrease (neg feedback from increased T3/T4);
Increase (continued secretion stimulated by hCG)

61
Q

Grave’s disease is an example of (primary/secondary) (X).

A

Primary;

X = Hyperthyroidism

62
Q

Exophthalmos is seen in (X) condition. What’s the reason for this?

A

X = hyperthyroidism;

Inflammation/swelling in orbital tissues (pushes eyeballs forward)

63
Q

Hashimoto’s disease is (primary/secondary) (X). What’s the central issue in this disease?

A

Primary;
X = hypothyroidism

Anti-thyroid Ab (autoimmune); leads to eventual destruction of thyroid gland

64
Q

What’s the mechanism behind swelling of (X) gland in Hashimoto’s disease?

A

X = thyroid

Inflitration of lymphocytes as well as fibrosis

65
Q

Silent, post-partum (X) condition begins with (hyper/hypo)-thyroidism, then (hyper/hypo)-thydroidism until normal function is reached again.

A

X = thyroiditis (inflammation of thyroid gland)

Hyper; hypo

66
Q

It’s a “rebound” or (increase/decrease) in (X) function that causes post-partum thyroiditis.

A

Increase;

X = immune system

Endo/Repro (15 decks)

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